Question

Prescribing exercise intensity can be achieved using many physiological variables. One of the most useful manners may be to use respiratory gas exchange measurements. First describe exercise intensity zones based upon ventilatory equivalents. Then relate the following: heart-rate zones, lactate threshold(s), and VO2max to these zones created using ventilatory equivalents.

Answer 1

First excersice intensity zones based upon ventilatory equivalents. During excersice, the amount of O2 entering the blood in the lungs is increased because amount of added to each unit of blood and the pulmonary blood flow per minute are increased. The P01 of blood flowing into the pulmonary capillaries falls from 40 to 25 mmHg or less, so that the alveolar capillary P02 gradient is increased and more O2 enters the blood. Blood flow per minute is increased from 5.5 L/min to as much as 20-35 L/min. The total amount of O2 entering the blood therefore increases from 250ml/min at rest to values as high as 4000ml/min. The amount CO2 excertion increases from 200ml/min to as much as 8000ml/min. The increase in O2 uptake is proportinate to work load up to a maximum. Above this maximum O2 consumption levels off and the blood lactate levels continue to rise. The lactate comes from muscles in which aerobic resynthesis of energy stores cannot keep pace with their utilization and an oxygen debt is being incurred. There is an abrupt increase in ventilation with the onset of excersice, followed after a brief pause by a further, more gradual increase is due mostly to an increase in the depth of respiration; this accompained by an increase in the respiratory rate when the excersice is more sternous. there is an abrupt decrease in ventilation when excersice ceases, followed after a brief pause by a more gradual decline to preexcersice values. the abrupt increase at the start of excersice is presumably due to psychic stimuli and afferent impulses from proprioceptors in muscles tendons and joints. The more gradual increase is presumably humoral even though afferial pH, Pco2 and Po2 remain constant during moderate excersice the increase in ventilation is proportinate to the increase in O2 consumption, but the mechanism responsible for the stimulatio of respiration. The increase in body temptreture may play a role, excersice increases the plasma K+ level, and this increase may stimulate the peripherel chemoreceptors. In addition it may be that the sensitivity of the respiratory center to CO2 is increased or that the respiratory fluctuations in arterial Pco, increase so that even though the mean arterial Pco2 does not rise, it is CO2 that is responsible for the increase in ventilation. O2 also seems to play some role despite the lack of a decrease in arterial Po2, since, during the performance of a given amount of work, the increase in ventilation while breathing 100%O2 is 10-20% less than the increase while breathing air. Thus, it currently appears that a number of deifferent factors combine to produce the increase in ventilation seen during moderate excersice.

When excersice becomes more vigrous, buffering of the increased amounts of lactic acid that are produced liberates more CO2 and this further increases ventilation. The response to graded excersice with increased production of acid, the increases in ventilation and CO2 production remain proportinate, so alveolar and arterial CO2 change relatively little. Because of the hyperventilation alveolar Po2 increases. with further accumulation of lactic acid, the increase in ventilation outstrips CO2 production and alveolar Pco2 falls, as does arterial Pco2. The decline in arterial Pco2 provides respiratory compensation for the metabolic acidosis produced by the additional lactic acid. The additional increase in ventilation produced by the acidosis is dependent on the carotid bodies and does not occur if they are removed. The respiratory rate after excersice does not reach basal levels until the O2 debt is reaid. This may take as long as 90 minutes thhe stimulus to ventilation after excersice is not the arterial Pco2 which is normal or low, or the arterial Po2 which is normal or high, but the elevated aterial H+ concentration due to the lactic acidemia. The magnitude exceeds basal consumption from the end of excertion until the O2 consumption has returned to preexcersice basal levels. During repayment of the O2 debt, there is a small rise in the O2 in muscle myoglobin. ATP and phosphorylcreatine are resynthesizes, and lactic acid is removed. Eighty percent of the lactic acid is converted to glycogen and 20% is metabolized to CO2 and H2O. Because of the extre CO2 produced by the buffering of lactic acid during sternous excersice, the R rises, reaching 1.5-2.0. Afterr exertion ehile the O2 debt is being repaid the R falls to 0.5 or less.